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Physiology of sleep and dreaming

Physiology of sleep and dreaming. The sleep cycle Dreaming Why do we sleep?. The sleep cycle. Electronic recording: EEG, EOG, EMG EEG patterns divide sleep into four stages: 1: a waves, 8 - 12 Hz, low amplitude, moderate frequency, similar to drowsy wakefulness

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Physiology of sleep and dreaming

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  1. Physiology of sleep and dreaming The sleep cycle Dreaming Why do we sleep?

  2. The sleep cycle • Electronic recording: EEG, EOG, EMG • EEG patterns divide sleep into four stages: • 1: a waves, 8 - 12 Hz, low amplitude, moderate frequency, similar to drowsy wakefulness • 2: slower frequency, higher amplitude, plus • K complexes • Sleep spindles • 3: d waves appear, 1-2 Hz, large amplitude • 4: Dominated by d waves

  3. REM sleep phenomena • Stage 1 EEG: Paradoxical sleep • EOG (and corneal bulge) show frequent eye movements, as if scanning a visual field. • EMG shows loss of muscle tonus due to downward inhibition of a motor neurons, although muscles moving hands and feet may twitch. • Many brain structures function as if awake.

  4. More REM phenomena • SNS is partially activated: Increases blood pressure, respiration, and heart rate. • Genital erection or partial erection: Postage stamp test. • Narrative dreaming • CBF is high to visual cortex, low to inferior frontal cortex (Madsen, 1991) • Eye movements match dream events • One EEG waveform is unique to REM and wakeful scanning

  5. Dream research • External stimuli may be incorporated into a dream. • Dream events happen in real time. • Everyone dreams; recall depends on when in the sleep cycle you awaken. • Genital response is independent of dream content. • Sleep-walking and talking are non-REM.

  6. Interpretation of dreams • Manifest content is symbolic of latent desires (Freud) • Activation-synthesis theory: cf. incorporation of external events into dreams. • Lucid dreams: Have you had one?

  7. Why do we sleep? • Restoration, recuperation or repair • Waking life disrupts homeostasis • Protection with the circadian cycle • Circadian synthesis

  8. Who sleeps? • Mammals and birds • Opossums, sloths, bats: 19-20 hours daily • Cats, dogs, rodents: 12-15 hours daily • Ruminant herbivores: 2-3 hours daily • Reptiles, amphibians, fish, and insects have cycles of inactivity • Note that sleep time does not correlate with waking activity levels, but does relate to waking vulnerability.

  9. Two interesting variations on sleep • Cetaceans • Indus dolphin • Bottlenose dolphin and porpoise • Flocking birds

  10. Circadian rhythms • Zeitgebers and the SCN • Free-running rhythms and the 25-hour period • Sleep deprivation within a circadian cycle is followed by less sleep, not more • Internal desynchronization: free-running body temperature cycle and sleep-wake cycle may desynchronize.

  11. Resynchronization • Jet lag and shift work • Phase shift: Delay is better than advance • Morning melatonin phase-delays • Afternoon melatonin phase-advances • Evening melatonin is ineffective • Bright light exposure has the opposite effects • Strengthen zeitgebers like light and activity early in the new waking period

  12. Sleep deprivation • Under total, voluntary sleep deprivation, sleepiness is cyclical • Greatest sleepiness from 3-6 a.m. • Waking sleepiness is countered by activity • Sleepiness increases only up to four days • Active, complex tasks are not impaired • Easy, boring tasks are impaired • Microsleep emerges

  13. Compensation for sleep deprivation • Subsequent slow-wave, non-REM sleep is increased • Stage 3 and 4 sleep is almost completely restored • Involuntary sleep deprivation is stressful • Executive rats on a carousel apparatus died • Post-mortem exams showed stress symptoms

  14. REM deprivation • REM pressure • REM rebound • REM escape • Three theoretical effects • Mental disorder • Amotivational syndrome • Memory processing deficits • But tricyclic antidepressants block REM with none of these side effects.

  15. Neural control of sleep • Is sleep a passive process? • The cerveau isole’ of Bremer (1936) • The encephale isole’ and the RAS • Partial transections leaving the RAS intact • Ventrolateral Preoptic Area (VPA) triggers sleepiness and slow-wave sleep • Warming the basal forebrain induces slow-wave sleep • VPA receives input from thermoreceptors

  16. More neural control • PGO waves in the EEG from implanted electrodes • Executive in the dorsolateral pons, called the peribrachial area. • Kainic acid lesions of peribrachial area reduce REM sleep • Carbachol, and ACh agonist, in ventral pons (medial pontine reticular formation) triggers REM phenomena.

  17. EEG patterns b 1 a 2 k 3 d 1 sec

  18. EEG patterns... 4 d 1 sec

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